Acetylcholine (ACh)

Product Details

Name Acetylcholine (ACh)
Alias 51-84-3; Acetylcholine; Choline acetate; O-Acetylcholine; Acetyl choline ion; Acetylcholinum;
CAS  No. 51-84-3
Category enzyme, protease
Weight 146.21 g/mol
Usage Reagents / experiment / Pharmaceuticals
Appearance White powder

Product Description

Acetylcholine (ACh) is a neurotransmitter. It is rapidly destroyed by cholinesterase in tissues. Acetylcholine can specifically act on various types of choline receptors, but its effects are wide and its selectivity is not high. Clinically, it is not used as a medicine, and it is generally only used as an experimental medicine. In nerve cells, acetylcholine is synthesized by choline and acetyl-CoA under the catalysis of choline acetyltransferase (choline acetylase). Mainstream studies suggest that increased levels of this substance in the human body are significantly associated with improved symptoms of Alzheimer's disease (Alzheimer's disease).

Function

Acetylcholine functions in both the central nervous system (CNS) and the peripheral nervous system (PNS). In the CNS, cholinergic projections from the basal forebrain to the cerebral cortex and hippocampus support the cognitive functions of those target areas. In the PNS, acetylcholine activates muscles and is a major neurotransmitter in the autonomic nervous system.

  • Cardiovascular system Parasympathetic nerves release ACh through its distal extremity to control cardiovascular system function, mainly producing the following effects:

(1) Vasodilation A small dose (20μg ~ 50 μg / min) of ACh can be administered to normal adults to dilate systemic blood vessels, including pulmonary vessels and coronary vessels. Its vasodilator effect is mainly due to stimulating vascular endothelial cell M3 choline receptor subtype, leading to the release of endothelium-derived relaxing factor (EDRF), namely nitric oxide (NO), which causes adjacent smooth muscle cells. relaxation. If the vascular endothelium is damaged, the above effects of ACh will no longer exist, which may cause vasoconstriction. In addition, the reduction of NA release from adrenergic nerve endings induced by ACh is also associated with vasodilation. A transient decrease in blood pressure due to vasodilation is often accompanied by an increase in reflex heart rate.
(2) slowing heart rate A large dose of ACh can slow down the heart rate, which is also called negative chronotropic action. This is related to the drug inhibiting atrioventricular node conduction. ACh can also delay the auto-depolarization of the sinus node during diastole, increase the repolarization current, and prolong the time to reach the action potential threshold. Causes the heart rate to slow down.
(3) Slowing down the atrioventricular node and Purkinje fiber conduction is a negative dromotropic action. ACh can prolong the refractory period of the atrioventricular node and Purkinje fibers and slow down their conduction. Complete cardiac blockade in cardiac glycosides or high-dose systemic administration of AChR agonists is often associated with significant inhibition of atrioventricular node conduction. The former can increase the vagal tone, that is, through ACh; the latter is the parasympathetic, that is, the pseudo-effect of ACh.
(4) Attenuating myocardial contractility is a negative inotropic action. Cholinergic nerves are mainly distributed in the sinoatrial node, atrioventricular node, Purkinje fiber and atrium, while the ventricles are less likely to have cholinergic innervation. Therefore, ACh is considered to have a greater inhibitory effect on atrial contraction than the ventricle. However, because the vagus nerve endings are closely adjacent to the sympathetic nerve endings, the ACh released by the vagus nerve terminals can stimulate the presynaptic mAChR of the sympathetic nerve terminals, and feedback suppresses the release of the sympathetic nerve endings NA, thus weakening the ventricular contractility.
(5) shortening the atrial refractory period ACh does not affect the conduction velocity of the atrial muscle, but can shorten the atrial refractory period and the action potential time course (that is, the vagus nerve action).
(6) The effects of cardiac ion channel ACh on cardiac ion channels are as follows: 1 increase K+ current (IK(ACh))2 in atrial myocytes, sinoatrial node and atrioventricular node cells to reduce slow inward Ca2+ current of cardiomyocytes (ICa) 3 attenuates the hyperpolarization activation current (If), which is related to diastolic depolarization. All of the above effects are associated with a slowing of the pace of cardiac pacing. Among them, 1 and 2 cause hyperpolarization of atrial cells and inhibit their contractility.

  • Gastrointestinal ACh can significantly excite the smooth muscle of the gastrointestinal tract, which increases the contraction amplitude and tension, increases the peristalsis of the smooth muscles of the stomach and intestines, and promotes the secretion of the stomach and intestines, causing symptoms such as nausea, belching, vomiting, and abdominal pain.
  • Urinary tract ACh can increase the smooth muscle peristalsis of the urinary tract, contraction of the bladder detrusor, increase the maximum voluntary voiding pressure of the bladder, reduce the bladder volume, and relax the bladder triangle and external sphincter to promote bladder emptying.
  • The other 1 gland ACh can increase the secretion of lacrimal gland, trachea and bronchial glands, salivary glands, digestive tract glands and sweat glands; 2 eyes can cause pupil contraction when AHT local eye drops, regulate myopia; 3 ganglia and skeletal muscle ACh can also act on the choline receptors of the autonomic ganglia and skeletal muscle neuromuscular junctions, causing sympathetic, parasympathetic ganglion excitation, muscle contraction; 4 central because ACh is not easy to enter the center, so although the central nervous system has choline receptors Exist, but peripheral administration rarely produces a central role; 5ACh can cause bronchoconstriction and excite the carotid and aortic chemical receptors.
Application

Human brain tissue has a large amount of acetylcholine, but the content of acetylcholine decreases with age. Normal elderly people are 30% lower than in youth, while those with dementia are more severe, reaching 70% to 80%. American doctor Wu Weman observed that the acetylcholine in the brain tissue of the elderly was reduced, and the elderly were given choline-rich foods, and it was found to have obvious effects of preventing memory loss. Scientists in countries such as the United Kingdom and Canada have also conducted research, agreeing that as long as the supply of adequate choline is controlled, the memory loss of the elderly in the 60s can be avoided. Therefore, maintaining and improving the content of acetylcholine in the brain is the fundamental way to solve the memory loss. In nature, acetylcholine is mostly present in the form of choline in eggs, fish, meat, soybeans, etc. These choline must be biochemically reacted in the human body to synthesize physiologically active acetylcholine. In addition, regular consumption of royal jelly can increase the content of acetylcholine in the brain, thereby promoting the activation of cranial nerve conduction function, improving the speed of information transmission, enhancing brain memory, comprehensively improving brain function, and delaying ageing.

Cardiovascular system ACh has the following effects on the cardiovascular system:

Synthesis and role of acetylcholine in synapses

(1) vasodilatation: intravenous injection of small doses of this product can cause a brief drop in blood pressure due to systemic vasodilation, accompanied by a reflex heart rate. ACh can cause many vasodilatations. Such as the lungs and coronary vessels. Its vasodilator effect is mainly due to inflammatory endothelial cells M, choline receptor subtype, leading to the release of endothelium-dependent relaxation factor (EDRF), nitric oxide (No), which causes relaxation of adjacent smooth muscle cells, possibly through Caused by baroreceptors or chemoreceptors. If the vascular endothelium is damaged, the above effects of ACh will no longer exist, which in turn may cause vasoconstriction. In addition, ACh inhibits the release of NA from noradrenergic nerve endings by activating the presynaptic M1 receptor of sympathetic nerve terminals and is also associated with ACh vasodilation.
(2) slow heart rate: also known as negative frequency effect. ACh can delay the auto-depolarization of the sinus node diastolic phase, increase the repolarization current, and prolong the action potential to reach the threshold, resulting in slow heart rate.
(3) slowing atrioventricular node and Pukenye fiber conduction: it is negative conduction. ACh can prolong the refractory period of the atrioventricular node and Βurkinje fibers, causing their conduction to slow down. Complete heart blockade that occurs when cardiac glycoside is used to increase vagal tone or systemic administration of high-dose choline receptor agonists is often associated with significant inhibition of atrioventricular node conduction.
(4) weakening myocardial contractility: that is, negative muscle strength. It is generally believed that cholinergic nerves are mainly distributed in the sinus node, atrioventricular node, Pukenye fiber and atrium, while the ventricle is less cholinergic innervation, so ACh inhibits atrial contraction more than the ventricle. However, because the vagus nerve endings are closely adjacent to the sympathetic nerve endings, ACh released from the vagus nerve terminals can stimulate the presynaptic M choline receptors in the sympathetic nerve terminals, and feedback suppresses the release of norepinephrine from the sympathetic nerve terminals. Reduces ventricular contractility.
(5) shortening the atrial refractory period: ACh does not affect the conduction velocity of the atrial muscle, but can shorten the atrial refractory period and the action potential duration (that is, the vagus nerve).

Gastrointestinal

ACh can obviously excite the smooth muscle of the gastrointestinal tract, increase its contraction amplitude, tension and peristalsis, and promote gastric and intestinal secretion, causing symptoms such as nausea, belching, vomiting, abdominal pain and defecation.
Urinary tract
ACh can increase the smooth muscle peristalsis of the urinary tract, contraction of the bladder detrusor, increase the maximum voluntary emptying pressure of the bladder, reduce the bladder volume, and relax the bladder triangle and the external sphincter, leading to bladder emptying.

other

(1) Gland: ACh can increase the secretion of lacrimal gland, trachea and bronchial glands, salivary glands, digestive tract glands and sweat glands.
(2) Eye: When ACh is partially instilled, it can cause the pupil to contract and adjust to myopia.
(3) ganglion and skeletal muscle: ACh acts on the NM choline receptors of the autonomic ganglia NN choline receptor and skeletal muscle neuromuscular junction, causing sympathetic, parasympathetic ganglion excitation and skeletal muscle contraction. In addition, because the adrenal medulla is innervated by sympathetic ganglion fibers, NN choline receptor agonism can cause adrenaline release.
(4) Central: Since ACh is not easy to enter the human center, although the central nervous system has choline receptors, peripheral administration rarely produces a central role.
(5) Bronchial: ACh can cause bronchoconstriction.
(6) ACh can also excite the carotid body and aortic body chemical receptors.

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